Figure 3. CXCL10 protein is upregulated in Tsc1^GFAPCKO mice and reversed by anti-inflammatory treatment in vivo and in vitro.

Protein expression of CXCL10 was assessed by western blotting in the brains and cultured astrocytes of Tsc1^GFAPCKO mice, and the effects of rapamycin and ECG were tested. (A) Vehicle-treated Tsc1^GFAPCKO mice have significantly increased CXCL10 levels, compared with control mice. Rapamycin treatment (3 mg/kg/d i.p. for seven days) significantly inhibited the upregulated-CXCL10 in Tsc1^GFAPCKO mice (7–11 mice/group). (B) Vehicle-treated cultured astrocytes from Tsc1^GFAPCKO mice showed increased CXCL10 expression compared with astrocytes from control mice. Rapamycin treatment (2 ng/ml added to the culture medium for 16 hours) blocked the up-regulation of CXCL10 in Tsc1^GFAPCKO astrocyte (n=8–12 mice/group). (C) Vehicle-treated Tsc1^GFAPCKO mice have significantly increased CXCL10 protein expression compared with control mice. ECG treatment (12.5 mg/kg/d i.p. for seven days) inhibited the increased CXCL10 in Tsc1^GFAPCKO mice, but this was still significantly higher than control mice (n=8 mice/group). * p<0.05, *** p<0.001, versus vehicle-treated control mice or astrocytes by one-way ANOVA; # p<0.05, ### p<0.001, versus vehicle-treated Tsc1^GFAPCKO mice or astrocytes by one-way ANOVA (n = 9–12 mice/group). Cont = control, KO = Tsc1^GFAPCKO, Veh = vehicle, Rap = Rapamycin, ECG = Epicatechin-3-gallate.